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L Aloe

Publications and source records attributed to L Aloe.

At least 145 records · Page 8Linked to original sources

Centrally injected nerve growth factor modulates peripheral immune responses in the rat.

The effect of the intracerebroventricular (icv) and intravenous (iv) injection of nerve growth factor (NGF) on peripheral immunity was studied in the rat. Icv administration of NGF (5, 25, 50, 250 and 500 ng/rat) significantly enhanced phytohemagglutinin (PHA)-induced splenocyte proliferation 30 min after treatment. Icv pretreatment with an anti-NGF antibody completely prevented the effect, while iv injection of anti-NGF antibody did not block the effect of icv NGF. On the contrary, NGF at doses of 0.5, 2.5, 5, 25 and 50 ng/rat decreased splenocyte natural killer (NK) activity. When injected iv, NGF enhanced splenocyte proliferation only at doses of 50 and 500 ng/rat, while it did not affect NK activity. These effects on immunity do not appear mediated by activation of the hypothalamus-pituitary-adrenal axis, since NGF did not modify plasma corticosterone concentrations at the doses used. These results indicate that NGF participates in the complex network of neuroimmune interactions.

Animals↗

Nerve growth factor circulating levels are increased in Kawasaki disease: correlation with disease activity and reduced angiotensin converting enzyme levels.

OBJECTIVE: To investigate the serum levels of nerve growth factor (NGF) and their possible relationship with disease activity in Kawasaki disease. METHODS: Twelve children with Kawasaki disease, 12 healthy children (afebrile controls), and 12 children with high fever related to upper respiratory tract viral infections (URTVI) were enrolled in the study. Serum NGF levels were measured by an ELISA method before and after therapy. In addition, angiotensin converting enzyme (ACE), and erythrocyte sedimentation rate (ESR), complete hemochrome, and C-reactive protein were tested as indicators of endothelial injury and disease activity, respectively. RESULTS: NGF levels were strikingly increased in the acute phase of Kawasaki disease (1219.54 +/- 1660.29 pg/ml) and decreased in the inactive phase of the disease (277.08 +/- 245.64 pg/ml), while remaining significantly higher than controls (6.5 +/- 2.03 pg/ml). In febrile patients with URTVI, NGF levels (30.18 +/- 44.70 pg/ml) were moderately but significantly increased compared to afebrile controls, but remarkably lower in respect to active and inactive Kawasaki disease. In active Kawasaki disease, ACE values were significantly lower than in healthy children (2.8 +/- 1.7 vs 10.1 +/- 4.2 pmol/ml/min; p < 0.001) and increased during the inactive phase, but remaining lower than in controls (4.8 +/- 2.7 pmol/ml/min); ESR, hemoglobin level, and platelet count showed significant correlation with NGF, while ACE levels showed a significant inverse correlation with ESR and NGF. CONCLUSION: In Kawasaki disease, NGF increased together with decreased ACE may be linked to a diffuse vascular inflammatory process. NGF and ACE levels remained abnormal even when there was no clinical sign of disease activity. This may indicate that the disease process is not in complete remission and suggests careful and prolonged cardiac followup until their normalization.

Child, Preschool↗

Monosodium glutamate increases NGF and NPY concentrations in rat hypothalamus and pituitary.

The effects of MSG treatment on NGF and NPY levels were analysed in the hypothalamus, pituitary, adrenal, thyroid and testis of adult rats. Daily i.v. injections of MSG (1 g kg-1 for 1 week) induced an increase of NGF in the hypothalamus (control (C) = 378 +/- 54; saline (S) = 369 +/- 36; MSG = 479 +/- 35 pg g-1 tissue; p < 0.001) and pituitary (C = 310 +/- 34; S = 376 +/- 114; MSG = 576 +/- 98 pg g-1 tissue; p < 0.01). Hypothalamic and pituitary NPY concentrations were also altered in the MSG-treated rats. Compared with saline-treated rats, the NPY concentration increased by 43% in the hypothalamus and 37.5% in the pituitary of MSG-treated rats. No significant changes in NGF and NPY content were found in the adrenal or thyroid of treated animals. These results suggest that hypothalamic and pituitary NGF and NPY levels may be involved in the control of neuroendocrine functions that are affected by MSG treatment.

Animals↗

Effect of NGF antibodies on mast cell distribution, histamine and substance P levels in the knee joint of TNF-arthritic transgenic mice.

We have previously shown an increase in nerve growth factor (NGF) levels and in mast cell (MC) distribution in the synovium of patients affected by rheumatoid arthritis. We now report that purified NGF antibodies injected into arthritic transgenic mice carrying the human tumour necrosis factor-alpha (TNF-alpha) gene caused reduction in the number of MCs, as well as a decrease in histamine and substance P levels within the synovium. These observations suggest that NGF antibody might be useful in studying the role of these pro-inflammatory markers in joint arthritis.

Animals↗

K-complexes: are they signs of arousal or sleep protective?

The number of K-complexes recorded at the central-temporal EEG derivation (C3-T3) during 5 min periods for both the ascending and descending phase of Stage 2 of NREM sleep for cycles 1, 2. etc. were counted in 10 subjects for each of the following five groups: normal persons, patients with a primary generalized form of epilepsy, narcolepsy, insomnia and obstructive sleep apnoea. The differences in time spent in different stages of sleep were as expected for these types of patients. A 2-within, 1-between factors, repeated measure ANOVA was applied to the data on K-complexes. Overall, there was no significant difference between the number of K-complexes observed during the ascending and descending phases of the different sleep cycles. Patients with a sleep disorder had significantly less well-defined K-complexes than the normals and the patients with a primary form of generalized epilepsy: for insomnia (P = 0.035), for apnoea (P = 0.011) and for narcolepsy (P = 0.001). There was a significant, but very low correlation coefficient between the number of K-complexes observed during Stage 2 of NREM sleep and the time spent during that stage for all groups combined (Rho 0.27, P = 0.002) and for the narcoleptic patients (Rho 0.44, P = 0.017). In all, the findings lend support to the hypothesis that a K-complex can be seen as a 'defensive response', or has a sleep protective function.

Journal Article↗

Changes in cerebral blood flow velocity associated with biofeedback-assisted relaxation treatment of migraine headaches are specific for the middle cerebral artery.

Twenty-five patients with diagnosed migraine headaches were randomly assigned to a biofeedback-assisted relaxation therapy group or to a group who relaxed on their own. This study confirmed that the biofeedback trained group significantly decreased pain and medication more than the self-relax group. The best responders were those with the more elevated initial cerebral blood flow values and the changes in cerebral blood flow were specific for the middle cerebral artery.

Adult↗

Elevated levels of nerve growth factor in the thalamus and spinal cord of rats affected by experimental allergic encephalomyelitis.

In a previous study it was shown that the levels of NGF in the cerebrospinal fluid of patients affected by multiple sclerosis (MS) increase during the acute phase of the disease and decrease in the remission phase. In the present study, using an animal model of MS, we investigate whether any changes in NGF levels occur in brains of rats affected by Experimental Allergic Encephalomyelitis (EAE). The results show an enhanced level of NGF in the thalamus and spinal cord and a numerical increase of mast cells (MCs) expressing mRNA-NGF localized in these two regions. These observations suggest that NGF is involved in EAE and that MCs contribute to the local increase of NGF.

Animals↗

Increased plasma levels of nerve growth factor in vernal keratoconjunctivitis and relationship to conjunctival mast cells.

PURPOSE: To evaluate the nerve growth factor (NGF) plasma concentration in patients with vernal keratoconjunctivitis and to correlate it with the histopathology and immunopathology of the disease. METHODS: An immunoenzymatic assay was performed to measure NGF plasma levels in patients with vernal keratoconjunctivitis and in healthy matched controls. A competitive radioimmunoassay was used to detect eosinophil cationic protein (ECP) and total specific immunoglobulin E (IgE) serum levels. Histologic evaluation was performed in tarsal and bulbar conjunctival biopsies. RESULTS: Plasma levels of NGF were significantly higher (P < 0.001) in patients with vernal keratoconjunctivitis (mean = 8224.47 +/- 7802.53 pg/ml; median = 121 pg/ml) than in controls (mean = 51.68 +/- 5.94 pg/ml; median 42.5 pg/ml). Conjunctival tissue showed a significant increase of mast cells, eosinophils, and lymphocytes in vernal keratoconjunctivitis. A significant correlation was observed between plasma levels of NGF and the number of mast cells in the tarsal conjunctiva (Cc = 0.81; P < 0.005) and bulbar conjunctiva (Cc = 0.77; P < 0.01) of patients with vernal keratoconjunctivitis. No correlation was found between NGF plasma levels and total IgE serum levels in patients with vernal keratoconjunctivitis; NGF plasma levels were inversely related to the number of circulating eosinophils (Cc = -0.61; P < 0.05) and to the increased serum levels of ECP (Cc = -0.71; P < 0.02). CONCLUSIONS: These data represent the first reported evidence of increased NGF plasma levels in an allergic human disease and suggest a possible relationship between this neurotrophic polypeptide and inflammatory cells in vernal keratoconjunctivitis.

Adolescent↗

Emotional stress induced by parachute jumping enhances blood nerve growth factor levels and the distribution of nerve growth factor receptors in lymphocytes.

We examined the plasma nerve growth factor (NGF) level and the distribution of NGF receptors in peripheral lymphocytes of young soldiers (mean age, 20-24 yr) experiencing the thrill of a novice about to make their first parachute jumps. Blood was collected from soldiers who knew they were selected to jump (n = 26), as well as from soldiers who knew they were not selected (n = 17, controls). The former group was sampled the evening before the jump and 20 min after landing. Compared with controls, NGF levels increased 84% in prejump and 107% in postjump sampling. Our studies also showed that the increase of NGF levels preceded the increase of plasma cortisol and adrenocorticotropic hormone. No changes in the baseline levels of circulating interleukin 1 beta or tumor necrosis factor were found, suggesting that the increased levels of NGF were not correlated with change in these cytokines. Moreover, immunofluorescence analysis demonstrated that parachuting stress enhances the distribution of low-affinity p75LNGFR and high-affinity p140trkA NGF receptors in circulating peripheral blood mononuclear cells. These observations suggest that the release of NGF might be involved in the activation of cells of the immune system and is most probably associated with homeostatic adaptive mechanisms, as previously shown for stressed rodents.

Adult↗

Schistosoma mansoni infection enhances the levels of NGF in the liver and hypothalamus of mice.

Schistosoma mansoni infection in adult mice is known to cause granulomas in the liver and intestine. Using a specific enzyme-linked immunoassay, it was found that Schistosoma mansoni infection enhances the level of nerve growth factor in the liver and surprisingly also in the hypothalamus. Exogenous administration of purified NGF antibodies inhibits NGF biological activity both in the hypothalamus and liver and drastically reduces the number of NGF-responsive cells, the mast cells, present in liver granuloma. These findings and those reported by others showing the effect of NGF on cells of the immune system support the hypothesis that this molecule plays a role in neuroendocrine-immune interactions.

Animals↗

Mast cells synthesize, store, and release nerve growth factor.

Mast cells and nerve growth factor (NGF) have both been reported to be involved in neuroimmune interactions and tissue inflammation. In many peripheral tissues, mast cells interact with the innervating fibers. Changes in the behaviors of both of these elements occur after tissue injury/inflammation. As such conditions are typically associated with rapid mast cell activation and NGF accumulation in inflammatory exudates, we hypothesized that mast cells may be capable of producing NGF. Here we report that (i) NGF mRNA is expressed in adult rat peritoneal mast cells; (ii) anti-NGF antibodies clearly stain vesicular compartments of purified mast cells and mast cells in histological sections of adult rodent mesenchymal tissues; and (iii) medium conditioned by peritoneal mast cells contains biologically active NGF. Mast cells thus represent a newly recognized source of NGF. The known actions of NGF on peripheral nerve fibers and immune cells suggest that mast cell-derived NGF may control adaptive/reactive responses of the nervous and immune systems toward noxious tissue perturbations. Conversely, alterations in normal mast cell behaviors may provoke maladaptive neuroimmune tissue responses whose consequences could have profound implications in inflammatory disease states, including those of an autoimmune nature.

Animals↗

Early exposure to aluminium affects eight-arm maze performance and hippocampal nerve growth factor levels in adult mice.

Aluminium has been implicated in the etiology of several human pathologies but, to date, little attention has been given to the potential damage caused by gestational exposure to aluminium or to any long-term effect of early exposure. Aluminium sulphate (200 mg/kg) was administered intraperitoneally to pregnant female mice (days 10 to 13 of gestation), and male progeny was assessed in a radial eight-arm maze task at 70 days (20 daily sessions, 50 microliters water as reward). Overall, aluminium-exposed mice performed less efficiently in the radial maze than the vehicle-exposed animals. Neurobiological data showed that aluminium mice also had a higher level of nerve growth factor in the hippocampal formation when compared to controls.

Aluminum↗

NGF effects on hot plate behaviors in mice.

Adult CD-1 male mice were injected intravenously with 2.5 micrograms/g of highly purified murine NGF and then assessed for hot plate responding (52 degrees C) at 15, 30, 60, 180, and 360 min (repeated test) or at 30, 60, or 360 min (single test, i.e., exposure to hot plate only once). Control animals received cytochrome c (2.5 micrograms/g). In the repeated test, NGF produced hyperalgesia, increasing the number of jumps (particularly at 30 and 60 min postinjection), while in the single test the pain reaction of NGF-treated animals remained unaffected. Sensitization of C-fibers in the periphery or release of bioactive mediators from mast cells may account for NGF-induced changes in nociception.

Animals↗

Cold water swimming stress alters NGF and low-affinity NGF receptor distribution in developing rat brain.

We have previously shown that the nerve growth factor (NGF) is released into the bloodstream following intraspecific fighting behaviour and that the level released correlates with the number of fighting episodes. We subsequently reported that NGF and its messenger RNA are present in identified hypothalamic nuclei and increase following intermale fighting behaviour. This report provides data showing that in 16-day-old rats cold water swimming stress (CWSS) alters the distribution of low-affinity NGF-Receptors (p75NGFR) and NGF levels in the central nervous system. A significant increase of NGF level was observed in the cortex, while the p75NGFR immunoreactivity decreased in neurons of the septum, nucleus basalis and striatum. Choline acetyltransferase activity in forebrain tissues remained at baseline levels. Our result suggests that NGF and p75NGFR, involved in the development and differentiation of the nervous system, are affected by stress.

Animals↗

Expression and function of nerve growth factor and nerve growth factor receptor on cultured keratinocytes.

Keratinocytes, a key cellular component both for homeostasis and pathophysiologic processes of the skin, secrete a number of cytokines and are stimulated by several growth factors. Nerve growth factor (NGF) is synthesized in the skin and basal keratinocytes express the low-affinity nerve growth factor receptor (NGF-R). We present evidence that normal human keratinocytes in culture express the low- and the high-affinity NGF-R both at the mRNA level, as determined by reverse-transcription polymerase chain reaction and at the protein level, as shown by cytofluorimetric analysis. NGF significantly stimulates the proliferation of normal human keratinocytes in culture in a dose-dependent manner. This effect can be prevented by the addition of both an anti-NGF neutralizing antibody and a high-affinity NGF-R (trk) specific inhibitor, the natural alkaloid K252a. By contrast, keratinocyte proliferation is not inhibited by an anti-low-affinity NGF-R monoclonal antibody, thus suggesting that NGF effect on human keratinocytes is mediated by the high-affinity NGF-R. Moreover, NGF mRNA is expressed in normal human keratinocytes and NGF is secreted by keratinocytes in increasing amounts during growth, as detected by enzyme-linked immunosorbent assay. These results suggest that NGF could act as a cytokine in human skin and take part in disorders of keratinocyte proliferation.

Antibodies, Monoclonal↗

Nerve growth factor and autoimmune diseases.

The initiation of a humoral immune response to a foreign antigen is a complex biologic process involving the interaction of many cell types and their secreted products. Autoimmune diseases, which are characterized by an abnormal activation of the immune system, probably result from the failure of normal self-tolerance mechanisms. The etiology of such illnesses, however, is far from being understood. While there have been extensive studies on the participation of the immune and endocrine systems in autoimmune diseases, few have dealt with nervous system-mediated immunoregulation in such situations. Evidence continues to grow suggesting that nerve growth factor (NGF), first identified for its activity in promoting the growth and differentiation of sensory and sympathetic neurons, may exert a modulatory role on neuroimmunoendocrine functions of vital importance in the regulation of homeostatic processes. Newly detected NGF-responsive cells belong to the hemopoietic-immune system and to populations in the brain involved in neuroendocrine functions. NGF levels are elevated in a number of autoimmune states, along with increased accumulation of mast cells. NGF and mast cells both appear to be involved in neuroimmune interactions and tissue inflammation. Moreover, mast cells themselves synthesize, store, and release NGF, proposing that alterations in normal mast cell behaviors may provoke maladaptive neuroimmune tissue responses whose consequences could have profound implications in inflammatory disease states, including those of an autoimmune nature. This review focuses on these cellular events and presents a working model which attempts to explain the close interrelationships of the neuroendocrinoimmune triade via a modulatory action of NGF.

Autoimmune Diseases↗

A proposed autacoid mechanism controlling mastocyte behaviour.

Evidence is provided here supporting the existence of a novel autacoid mechanism negatively modulating mast cell behaviour in response to noxious stimuli in vivo; hence, the denomination "autacoid local inflammation antagonism" (ALIA). In particular, as lipid amides of the N-acylethanolamine type have been reported to accumulate in tissues in degenerative inflammatory conditions, we examined whether these N-acylated lipids could exert regulatory effects on mast cell activation in vivo. The results reported show that both long- and short-chain N-acylethanolamines, when systemically administered, are effective in reducing mast cell degranulation induced by local injection of substance P in the ear pinna of developing rats. These and other data suggest that the endogenous production of N-acylethanolamines may constitute a local autocrine/paracrine response for the negative feedback control of mast cell responses to various activating signals. Such a process may be of physio-pathological relevance in the regulation of functional neuro-immune-mast cell interactions.

Animals↗

Postnatal cocaine exposure affects neonatal passive avoidance performance and cholinergic development in rats.

Wistar rat pups received either cocaine HCl (25 mg/kg) or saline (0.9% NaCl) SC from postnatal days 1-11. On days 12 (acquisition) and 13 (retention), they underwent a passive avoidance task (step-off response; grid foot-shock at 0.35 mA). Slight deficits were found in cocaine-treated subjects for latency to step-off during acquisition and for generalized increase in the number of trials to criterion in retention. On postnatal day 13, the level of choline acetyltransferase (ChAT) enzymatic activity and the distribution of ChAT neuronal immunoreactivity in forebrain structures were examined. These morphometric and biochemical studies demonstrate a decrease of cholinergic enzymes in the septum, while the remaining basal forebrain cholinergic regions were unaffected.

Animals↗